Rigid Ryegrass (Lolium rigidum) is a monocot weed in the Poaceae family. In South Australia this weed first evolved multiple resistance (to 7 herbicide sites of action) in 1982 and infests Spring Barley, and Wheat. Multiple resistance has evolved to herbicides in the Groups A/1, B/2, K1/3, K2/23, K3/15, N/8, and F4/13. These particular biotypes are known to have resistance to chlorpropham, chlorsulfuron, clomazone, diclofop-methyl, ethalfluralin, fluazifop-P-butyl, imazapyr, metolachlor, metsulfuron-methyl, quizalofop-P-ethyl, sethoxydim, tralkoxydim, triallate, triasulfuron, and trifluralin and they may be cross-resistant to other herbicides in the Groups A/1, B/2, K1/3, K2/23, K3/15, N/8, and F4/13.

The 'Group' letters/numbers that you see throughout this web site refer to the classification of herbicides by their site of action. To see a full list of herbicides and HRAC herbicide classifications click here.

Cross-resistance to numerous herbicides, including chloracetamides. It should be noted that not all biotypes have resistance to each of the herbicides listed. The most common resistances are to ACCase inhibitors and ALS inhibitors.

Field, and Greenhouse trials comparing a known susceptible Rigid Ryegrass biotype with this Rigid Ryegrass biotype have been used to confirm resistance. For further information on the tests conducted please contact the local weed scientists that provided this information.

Genetics

Genetic studies on Group A, B, K1, K2, K3, N, F4/1, 2, 3, 23, 15, 8, 13 resistant Rigid Ryegrass have not been reported to the site. There may be a note below or an article discussing the genetics of this biotype in the Fact Sheets and Other Literature

Mechanism of Resistance

Studies on the mechanism of resistance of multiple resistant Rigid Ryegrass from South Australia indicate that resistance is due to an altered target site, and enhanced metabolism. There may be a note below or an article discussing the mechanism of resistance in the Fact Sheets and Other Literature

Relative Fitness

There is no record of differences in fitness or competitiveness of these resistant biotypes when compared to that of normal susceptible biotypes. If you have any information pertaining to the fitness of multiple resistant Rigid Ryegrass from South Australia please update the database.

University Of Adelaide - Waite CampusCrc For Australian Weed Management And School Of AgricultureBox 2146Adelaide, 5064, South AustraliaAustralia Email Christopher Preston

ACKNOWLEDGEMENTS

The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in South Australia have been instrumental in providing you this information. Particular thanks is given to Christopher Preston for providing detailed information.

Herbicide resistance in rigid ryegrass is an escalating problem in grain-cropping fields of southeastern Australia due to increased reliance on herbicides as the main method for weed control. Weed surveys were conducted between 1998 and 2009 to identify the extent of herbicide-resistant rigid ryegrass across this region to dinitroaniline, and acetolactate synthase- and acetyl coenzyme A (CoA) carboxylase-inhibiting herbicides. Rigid ryegrass was collected from cropped fields chosen at random. Outdoor pot studies were conducted during the normal winter growing season for rigid ryegrass with PRE-applied trifluralin and POST-applied diclofop-methyl, chlorsulfuron, tralkoxydim, pinoxaden, and clethodim. Herbicide resistance to trifluralin in rigid ryegrass was identified in one-third of the fields surveyed from South Australia, whereas less than 5% of fields in Victoria exhibited resistance. In contrast, resistance to chlorsulfuron was detected in at least half of the cropped fields across southeastern Australia. Resistance to the cereal-selective aryloxyphenoxypropionate-inhibiting herbicides diclofop-methyl, tralkoxydim, and pinoxaden ranged between 30 and 60% in most regions, whereas in marginal cropping areas less than 12% of fields exhibited resistance. Resistance to clethodim varied between 0 and 61%. Higher levels of resistance to clethodim were identified in the more intensively cropped, higher-rainfall districts where pulse and canola crops are common. These weed surveys demonstrated that a high incidence of resistance to most tested herbicides was present in rigid ryegrass from cropped fields in southeastern Australia, which presents a major challenge for crop producers..

Two field experiments were undertaken at Roseworthy, South Australia from 2006 to 2007 to evaluate the performance of herbicide application strategies for the control of herbicide-resistant rigid ryegrass in faba bean grown in wide rows (WR). The standard farmer practice of applying postsowing PRE (PSPE) simazine followed by POST clethodim to faba bean grown in WR provided consistent and high levels of rigid ryegrass control (≥96%) and caused a large reduction (P<0.05) in spike production (≤20 spikes m-2) as compared with nontreated control (560 to 722 spikes m-2). Furthermore, this herbicide combination resulted in greatest yield benefits for WR faba bean (723 to 1,046 kg ha-1). Although PSPE propyzamide used in combination with shielded interrow applications of glyphosate or paraquat provided high levels of rigid ryegrass control (≥93%), these treatments were unable to reduce ryegrass spike density within the crop row (20 to 54 spikes m-2) to levels acceptable for continued cropping. Furthermore, a yield reduction (13 to 29%) was observed for faba bean in treatments with shielded application of nonselective herbicides and could be related to spray drift onto lower leaves. These findings highlight that shielded interrow spraying in WR faba bean could play an important role in the management of rigid ryegrass in southern Australia. However, timing of shielded interrow applications on weed control, crop safety, and issues concerning integration with more effective early-season control strategies require attention..

Acetolactate Synthase- (ALS) inhibiting herbicides are important components for the control of ryegrass species infesting cereal-cropping systems worldwide. Although resistance to ALS herbicides in ryegrasses has evolved more than 25 yr ago, few studies have been dedicated to elucidate the molecular mechanisms involved. To this end, we have investigated the molecular basis of chlorsulfuron, sulfometuron-methyl, and imazapyr resistance in AUS5 and AUS23, two ryegrass populations from Australia. Comparison between whole-plant herbicide assays and DNA sequencing results showed that resistance to the nonmetabolizable herbicide sulfometuron-methyl was associated with four different proline mutations at ALS codon position 197 (P197) in AUS23. In addition to three P197 amino acid changes impacting on the efficacies of the two sulfonylurea herbicides, the tryptophan to leucine target-site mutation at ALS codon position 574 (W574L) was present in AUS5, conferring resistance to both sulfometuron-methyl and imazapyr. The samples were also characterized by non target-site-based resistance impacting on the metabolizable herbicide chlorsulfuron only. Interestingly, compound mutant heterozygotes threonine/serine at ALS position 197, and plants with double mutations at positions 197 and 574 were detected, thus reflecting the ability of this outcrossing species to accumulate mutant alleles. Whole-plant dose-response assays conducted on predetermined wild-type and mutant genotypes originating from the same populations allowed for a more precise estimation of the dominant and very high levels of resistance associated with the proline to serine target-site mutation at ALS codon position 197 (P197S) and W574L mutations. The two highly efficient polymerase chain reaction- (PCR) based derived cleaved amplified polymorphic sequence (dCAPS) markers developed here will allow for quick confirmation of 197 and 574 ALS target-site resistance in ryegrass species field samples and also contribute to identify populations characterized by other likely resistance mechanisms in this important weed species.

An account is given of management methods to control herbicide-resistant populations of annual ryegrass (Lolium rigidum) in southern Australia. Some farmers use a pasture phase (2-3 years) with sheep grazing and non-selective herbicides to deplete the weed seed bank. In low-to-medium rainfall zones farmers combine cultural control with the use of alternative herbicides, mainly trifluralin. Cultural practices include delayed sowing (sometimes in conjunction with a shallow autumn cultivation), stubble burning, hay cutting or use as green manure, increased crop density and capture of weed seeds at harvest. The selection of crop species and cultivars with superior weed suppression potential is also discussed..

The biotype WLR1, that had been treated with the sulfonylurea herbicide chlorsulfuron in 7 consecutive years, was resistant to both wheat-selective and non-selective sulfonylurea and imidazolinone herbicides. Biotype SLR31, which became cross-resistant to chlorsulfuron following treatment with the aryloxyphenoxypropionate herbicide diclofop-methyl, was resistant to the wheat-selective, but not non-selective, sulfonylurea and imidazolinone herbicides. The concentrations of herbicide required to reduce in vitro acetolactate synthase (ALS) activity by 50% with respect to control assays (without herbicide) were greater for WLR1 than for susceptible VLR1 by a factor of >30, >30, 7, 4, and 2 for the herbicides chlorsulfuron, sulfometuron-methyl, imazapyr, imazethapyr, and imazamethabenz, respectively. ALS activity from SLR31 responded in a similar manner to that of the susceptible VLR1. Resistant biotypes metabolized chlorsulfuron more rapidly than the susceptible biotype. Metabolism of 50% of [phenyl-U-14C] chlorsulfuron in the culms of two-leaf seedlings required 3.7 h in SLR31, 5.1 h in WLR1, and 7.1 h in VLR1. In all biotypes the metabolism of chlorsulfuron in the culms was more rapid than that in the leaf lamina. Resistance to ALS inhibitors in L. rigidum may involve at least two mechanisms, increased metabolism of the herbicide and/or a herbicide-insensitive ALS..

Glyphosate is a broad-spectrum systemic herbicide used to kill weeds, especially annual broadleaf weeds and grasses known to compete with commercial crops grown around the globe. However, weeds evolve and develop resistance to glyphosate. Until recently, no case of glyphosate resistance had been detected in France. Glyphosate resistance was indeed recently recorded in a Lolium rigidum weed population from a vineyard in the South of France. Here, we studied the mechanisms of this resistance case. Seed samples of L. rigidum were collected from the vineyard where resistance had been detected, as well as from a nearby area that had no known history of exposure to glyphosate. We studied the effect of retention of glyphosate spray, shikimic acid accumulation, glyphosate absorption and translocation, glyphosate metabolism, and the sequence of the enzyme that glyphosate targets in plants, 5-enolpyruvylshikimate-3-phosphate synthase. Our results show that glyphosate absorption decreased by 30 % in the resistant L. rigidum weed. In addition, glyphosate translocation out of the treated leaves was reduced by 52 %. Finally, the resistant biotype had a serine amino acid substitution at position 106 of the predicted protein, instead of the proline amino acid present in the susceptible population. Our results suggest that the resistant population of L. rigidumpresents three different mechanisms of resistance to glyphosate, namely reduced absorption, reduced mobility in the plants, and a mutation in the gene coding for the enzyme targeted by glyphosate..

Populations of rigid ryegrass with resistance to glyphosate have started to become a problem on fence lines of cropping fields of southern Australian farms. Seed of rigid ryegrass plants that survived glyphosate application were collected from two fence line locations in Clare, South Australia. Dose-response experiments confirmed resistance of these fence line populations to glyphosate. Both populations required 9- to 15-fold higher glyphosate dose to achieve 50% mortality in comparison to a standard susceptible population. The mechanism of resistance in these populations was investigated. Sequencing a conserved region of the gene encoding 5-enolpyruvyl-shikimate-3-phosphate synthase identified no differences between the resistant and susceptible populations. Absorption of glyphosate into leaves of the resistant populations was not different from the susceptible population. However, the resistant plants retained significantly more herbicide in the treated leaf blades than did the susceptible plants. Conversely, susceptible plants translocated significantly more herbicide to the leaf sheaths and untreated leaves than the resistant plants. The differences in translocation pattern for glyphosate between the resistant and susceptible populations of rigid ryegrass suggest resistance is associated with altered translocation of glyphosate in the fence line populations..

Agricultural weeds have rapidly adapted to intensive herbicide selection and resistance to herbicides has evolved within ecological timescales. Yet, the genetic basis of broad-spectrum generalist herbicide resistance is largely unknown. This study aims to determine the genetic control of non-target-site herbicide resistance trait(s) that rapidly evolved under recurrent selection of the novel lipid biosynthesis inhibitor pyroxasulfone in Lolium rigidum. The phenotypic segregation of pyroxasulfone resistance in parental, F1 and back-cross (BC) families was assessed in plants exposed to a gradient of pyroxasulfone doses. The inheritance of resistance to chemically dissimilar herbicides (cross-resistance) was also evaluated. Evolved resistance to the novel selective agent (pyroxasulfone) is explained by Mendelian segregation of one semi-dominant allele incrementally herbicide-selected at higher frequency in the progeny. In BC families, cross-resistance is conferred by an incompletely dominant single major locus. This study confirms that herbicide resistance can rapidly evolve to any novel selective herbicide agents by continuous and repeated herbicide use. The results imply that the combination of herbicide options (rotation, mixtures or combinations) to exploit incomplete dominance can provide acceptable control of broad-spectrum generalist resistance-endowing monogenic traits. Herbicide diversity within a set of integrated management tactics can be one important component to reduce the herbicide selection intensity..

The study aimed to determine the usefulness of isothermal calorimetry and FT-Raman spectroscopy for the early evaluation of rigid ryegrass resistance to fenoxaprop-P ethyl (active ingredient one of aryloxyphenoxypropionate herbicides). The calorimetric measurements were done on the 4-day-old seedlings of susceptible and resistant biotypes of rigid ryegrass (Lolium rigidum Goud.) for 72 h, at 20°C. It was observed that the specific thermal power-timecurves of the susceptible and resistant biotypes growing on water (control) were qualitatively similar. Herbicides changed the shape of the specific thermal power-time curves of both biotypes. Furthermore, the total specific thermal energy was significantly higher for the seedlings of resistant biotype, growing both on water or herbicide, as compared to the susceptible ones. The analysis of the seedlings' endosperm, conducted using FT-Raman spectroscopy, showed a weaker intensity of the bands in the spectra derived from the resistant biotype. Differences in the specific thermal power-time curves and FT-Raman spectra between susceptible and resistant biotypes growing on water indicate that the sensitive and resistant biotypes are metabolically and chemically different already in the early stages of the seedling growth. We conclude that isothermal calorimetry and FT-Raman spectroscopy are efficient tools for the early detection of rigid ryegrass resistance to fenoxaprop-P ethyl..

Resistance to the acetyl-coenzyme A carboxylase (ACCase)-inhibiting herbicides in Lolium rigidum is widespread in grain cropping areas of South Australia. To better understand the occurrence and spread of resistance to these herbicides and how it has changed with time, the carboxyl transferase (CT) domain of the ACCase gene from resistant L. rigidum plants, collected from both random surveys of the mid-north of Southern Australia over 10 years as well as stratified surveys in individual fields, was sequenced and target site mutations characterised. Amino acid substitutions occurring as a consequence of these target site mutations, at seven positions in the ACCase gene previously correlated with herbicide resistance, were identified in c. 80% of resistant individuals, indicating target site mutation is a common mechanism of resistance in L. rigidum to this herbicide mode of action. Individuals containing multiple amino acid substitutions (two, and in two cases, three substitutions) were also found. Substitutions at position 2041 occurred at the highest frequency in all years of the large area survey, while substitutions at position 2078 were most common in the single farm analysis. This study has shown that target site mutations leading to amino acid substitutions in ACCase of L. rigidum are widespread across South Australia and that these mutations have likely evolved independently in different locations. The results indicate that seed movement, both within and between fields, may contribute to the spread of resistance in a single field. However, over a large area, the independent appearance and selection of target site mutations conferring resistance through herbicide use is the most important factor..